Contact: +91-22-2387 8000
+91-22-2386 4652

Dr. A. K. Chaudri

The vertebral arteries are branches of the subclavian arteries. Together with the basilar artery constitute the vertebrobasilar system which supplies blood to the posterior part of Circle of Willis and anastomose with blood supplied to the anterior part of the circle of Willis from the carotid arteries.

Cranial portion of the Vertebral arteries

Inside the skull, the two vertebral arteries join up to form the basilar artery at the base of the medulla oblongata. The basilar artery is the main blood supply to the brain stem and connects to the Circle of Willis to potentially supply the rest of the brain if there is compromise to one of the carotids.

Cervical portion of the Vertebral arteries – Can be divided into 4 parts for the purpose of description

I. TUBOTYMPANIC DISEASE (SAFE TYPE)
Etiology:
i. Residue of an acute otitis media infection during childhood.
ii. Repeated infections from the eustachian tube.
Perforation – Usually in the form of a central perforation situated exclusively in the pars tensa.
The ossicular chain often remains intact and middle ear mucosa is pink and edematous.

Clinical features:
1. Discharge – is mucoid, copious and non foul smelling. It becomes profuse during an upper respiratory infection.
2. Deafness – is conductive in type. Degree varies with the position and size of perforation.

Anatomy and Physiology of the Ear Click here
Perforation of the Ear Drum (Tympanic membrane)

A perforated eardrum is a hole or rupture in the ear
drum, the thin membrane that separates the ear canal
and the middle ear.

The Ear drum can perforate from infection or trauma.

An Infective perforation of the eardrum
Starts with infection from the nose after a head cold travelling up the Eustachian tube to reach the middle ear to promote an infection in the middle ear. Pus builds up in the middle ear behind the ear drum with pressure causing severe throbbing pain and breaks through a weak point in the ear drum leaving a perforation with a discharge of pus or blood.

A Traumatic perforation of the eardrum may occur:

– By a slap on the ear
– As part of a skull fracture
– After a sudden explosion from a bomb blast or fire cracker blast
– Insertion of a pin, cotton bud or stick if pushed too far into the ear canal.
A traumatic perforation usually has irregular shape and size and irregular edges.

A Traumatic perforation Photograph of the left ear drum of a patient K. E., after a Bomb blast in Mumbai

Symptoms and Signs of a Ear drum perforation: A perforated eardrum is usually accompanied by decreased hearing, occasional discharge, tinnitus and sometimes vertigo. Pain is usually not present.

Diminished hearing

Due to loss of drum surface area, less sound vibrations reach the middle ear and internal ear with resulting deafness. It is difficult to determine the location of the source of sound – that is directional (stereophonic) hearing is difficult. Appreciation of stereophonic music is affected.
When old age deafness sets in due to age related changes of the organ and nerves of hearing, the additional hearing impairment in the affected ear would be more pronounced than in the better hearing ear and becomes a definite handicap in communication.

Usually, the larger the perforation, the greater the loss of hearing. If disruption of the chain of bones in the middle ear occurs less sound is transmitted to the inner ear, the loss of hearing is more severe. The type of of deafness is of the Conductive type.

If the perforated eardrum is due to a sudden severe trauma (e.g. skull fracture) traumatic or explosive event like a cracker or bomb blast, because of shake up of the ultra microscopic hair cells in the inner ear, the hearing loss may be very pronounced – a mixed hearing loss from a summation of the conductive component – ear drum perforation and dislocation of the small bones in the middle ear and a sensori neural component due to inner ear damage. from damage to the inner ear structures,
Rarely, a long standing perforation may be the precursor of a cholesteatoma

Recurrent Eardischarge

A perforation of the ear drum creates a system of a tube open at both ends. Water, oil or even ear drops instilled into the ear can flow freely from the external ear into the middle ear and into the back of the nose and throat by the eustachian tube. Conversely, nasal discharge can flow freely from the back of the nose via the eustachian tube into the middle ear and come out through the perforation into the external ear.
As long as the perforation remains, there is therefore, a chance of getting recurrent ear discharge. This can happen every time after catching a cold since blowing the nose forces nasal discharge into the middle ear. It also happens if water accidentally enters the ear as during a bath or during swimming when the infected water comes into contact with the delicate lining of the middle ear and excites an inflammation (otitis media) with resulting ear discharge.

Tinnitus (Noise in th Ear)

A continuous or intermittent noise in the ear can be present. This usually disappears after closure of the perforation by surgery.

Vertigo

Continuous or intermittent episodes of vertigo may occur, since the organ of hearing and balance are one anatomically connected organ.

Natural course of a Ear drum perforation

Eardrum perforations of small size may heal spontaneously in a few weeks.
Medium sized perforations may or may not heal on their own.
Large perforations cannot heal on their own and require surgery.

The benefits of closing a perforation include prevention of recurrent middle ear infection by preventing water entering the middle ear while showering, bathing, or swimming (which could cause ear infection), improved hearing, and diminished tinnitus. It also may prevent the development of cholesteatoma (skin cyst in the middle ear), which can cause chronic infection and destruction of ear structures.

A small perforation can be kept under observation to see if it could close spontaneously. or try to cauterize the edges of the perforation under the operating microscope, with a chemical to stimulate growth of epithelium from the surrounding area to grow over the perforation. If healing is not achieved, surgery has to be considered.

A large or moderate sized perforation requires a surgical operation (Tympanoplasty or Myringoplasty) to close it. There are a number of surgical techniques, all of which aim at placing a piece of fascia covering the Temporalis muscle across the perforation. Surgery is typically quite successful in closing the perforation permanently, and improving hearing.

By a small incision within the ear canal, the ear drum perforation edges are freshened. The ear drum has 3 layers. These layers are gently separated under an operating microscope. A tissue graft (temporalis fascia) is obtained by a small separate incision above the ear (requiring one stitch). This is placed carefully in between the ear drum layers. The operation is performed under local anaesthesia with sedation. Hospitalization is for a few hours.

Water or oil should not enter the ear at all. Before a bath, the ear canal is sealed with a cotton ball smeared with vaseline or any other hair dressing. Wash hair with head hanging down under a running tap. Dry well with a towel before standing up again.

Swimming is NOT advisable at all, till the perforation has been closed by surgery. If you have to swim, do so without dipping the head under water. No diving at all.

Do NOT allow your ear to be syringed by your doctor at all.

Do NOT use towel corners, match sticks, hair grips to clear the ear. They provoke infection

Do not blow the nose when you have a head ‘cold’. This will drive the nasal discharge into the middle ear via the Eustachian tube and start a ear discharge. To clear nasal discharge, sniff in and throw out the discharge through the mouth. If you sneeze, do so with mouth open.

If there is any itching in the ears or you feel the need to clean the ear, do so with cotton buds only after smearing an antibiotic-antifungal cream like Surfaz SN cream

Every time you catch a ‘cold’, there is a likelihood of recurrence of ear discharge. Hence avoid iced water, ice creams, cold drinks etc. Avoid undue exposure to cold.

On catching a cold, immediate treatment from the family physician is started.

Chronic Otitis Media is a chronic infection (ear infection lingering on for over 3 months’ duration) of the middle ear cleft. It This includes disease of the middle due to infections by bacteria, virus etc. It may be Suppurative (with pus formation) or Non suppurative (without the formation of pus).

Chronic Non-Suppurative Otitis Media – Also known as Serous or Secretory Otitis Media or Otitis media with effusion (OME)

Chronic Suppurative Otitis Media of the Unsafe type

ATTICO – ANTRAL or MARGINAL TYPE (UNSAFE TYPE)

It is associated with formation of cholesteatoma and therefore regarded as unsafe. The term cholesteatoma is not an accurate description as it is not a tumour and always does not contain cholesterol chrystals. A cholesteatoma, truly speaking is ‘skin in the wrong place’ (Gray). This usually affects the postero-superior quadrant of ear drum (pars tensa) or the attic or epitympanum (Pars flaccida).

A cholesteatoma starts life as a dimple due to localised retraction of a portion of the tympanic membrane in the attic or postero superior quadrant of the pars tensa. It is in reality a retraction pocket and not a “perforation”. Epithelial squames (flat cells of skin) acumulate inside the dimple which soon shuts off and presents as an expanding bag. As more and more epethilium accumulates within the bag, the cholesteatoma forms an expanding erosive bag. This has the potential of eroding bone. Erosion of the small bones of the middle ear – ossicles result in conductive deafness. If it erodes the labyrinth, a sensori neural deafness ensues. Erosion of the facial nerve canal can lead to facial muscle paralysis. Erosion of the labyrinth can cause vertigo. When it grows superiorly, it can erode the tegmen tympani and cause intra cranial complications like meningitis and brain abscess.

Classification:

1. Congential:- originates as embryonic rest cells, which eats away the bone until it breaks through the outer attic wall. The ear drum is normal in the initial stages. Derlaki and Clemis defined congenital cholesteatoma or Primary choleasteatoma as an embryonic rest of epithelial tissue in an ear without tympanic membrane perforation, in a patient without history of ear infection.

a) Immigration - Of tympanic epithelium on deep meatal skin in the posterior superior quadrant of the tympanic membrane occurs. This is possible following destruction of the annulus after a previous middle ear discharge.

b) Metaplasia - Is provoked by chronic infection in the ciliated mucous membrane of the middle ear. Here squamous metaplasia occurs as well as there can be a marginal migration of squamous epithelium from the meatus.

Over time, untreated cholesteatoma can lead to bone erosion and spread of the ear infection to localized areas such as the inner ear and brain causing deafness, facial muscle paralysis, brain abscess, meningitis, and even death can occur.

Formation of a Cholesteatoma (Pathogenesis)

A cholesteatoma usually occurs because of poor eustachian tube function as well as infection in the middle ear. The eustachian tube normally conveys air from the back of the nose into the middle ear to equalize ear pressure. When the eustachian tubes works poorly perhaps due to allergy, a cold or sinusitis, the air in the middle ear is absorbed by the body, and a partial vacuum results in the ear. The vacuum pressure sucks in a pouch or sac by stretching the eardrum inwards, especially the superior part of the pars tensa or pars flaccida of the ear drum or areas weakened by previous infections.

Cholesteatomas It usually takes the form of a cyst or pouch that containing scales of accumulated skin arranged in onion – like layers.

Symptoms of a Cholesteatoma

Initially, the ear may discharge off and on. The discharge may have a characteristic foul odour. As the cholesteatoma pouch or sac enlarges, it can cause a full feeling or pressure in the ear, along with hearing loss. Dizziness due to involvement of the balance organ and facial muscle weakness on the same side as the cholesteatoma can occur. Ideally, urgent evaluation is required as soon as the diagnosis of cholesteatoma is made.

Dangers of ignoring a Cholesteatoma

Ear cholesteatomas can be dangerous because of their ability to erode bone.They occur in an area crowded with important structures. There is only a thin plate of bone separating a cholesteatoma from the brain and meninges and lie close to the small bones (ossicles) of the middle ear, the organ of hearing and balance in the internal ear, facial nerve. should never be ignored. Bone erosion can cause the infection to spread into the surrounding areas, including the inner ear and brain. If untreated, deafness, brain abscess, meningitis, and rarely death can occur.

These are indicated by headache, giddiness, increasing deafness and noises in the ear and weakness of the facial muscles. Over time, the cholesteatoma sac increases in size, the mouth of the sac being blocked by skin flakes. With expansion, it starts eroding surrounding structures of the middle ear

Progression of Cholesteatoma & Chronic mastoiditis and Complications

Treatment of Chronic Mastoiditis and Cholesteatoma

Hearing and balance tests, CT scans of the mastoid bone may be necessary to determine the hearing level and the extent of destruction the cholesteatoma has caused.

A cholesteatoma usually requires surgical treatment to prevent serious complications. Surgery (called Tympano- Mastoidectomy involving extensive bone drilling of the mastoid bone and removal of disease from the middle ear is required. It may be performed under general or local anesthesia. The primary purpose of surgery is to remove the cholesteatoma and infection and achieve an infection-free, self-cleansing dry ear. Hearing preservation or restoration is a secondary goal of surgery. If the disease has been satisfactorily removed. The small bones of the middle ear are repositioned to restore the hearing. Various inert material prosthesis of teflon, stainless steel, silicone and hydroxyapetite as well as homo or auto graft of bone and cartilage may also be used. In cases of severe ear destruction, restoration of normal hearing may not be possible. Reconstruction of the middle ear to its normal anatomy is usually not possible in one operation; and therefore, a second operation (if deemed necessary) may be performed later. Facial nerve repair or procedures to control dizziness are rarely required.

Follow-up office visits after surgical treatment are necessary and important, because cholesteatoma sometimes recurs. In cases where an open mastoidectomy cavity has been created, office visits every few months are needed in order to clean out the mastoid cavity and prevent new infections. In some patients, there must be lifelong periodic ear examinations.

Mechanism of Eustachian tube obstruction

Nature’s mechanism of ventilating the middle ear through the nose to maintain air on the inner side of the ear drum has disadvantages. All nasal diseases and Endoscopic view of fluid conditions can cause infective and obstructive symptoms affecting middle and bubbles behind ear drum ear function – e.g. common colds, viral and bacterial infections of the nose. .

Obstruction at the nasal end of the tube can be caused by by enlarged adenoids, tumours, infected water during swimming, pressure changes during air travel and diving under water. Chronic nasal allergy accounts for a sizeable number of patients suffering from Eustachian tubal obstruction.

When tubal obstruction remains for long, a vacuum forms. Fluid pours into the middle ear (Secretory Otitis Media). The fluid is thin initially and later as days go by, it becomes thick like glue (gum), when the condition is called ‘glue ears’.

How is the diagnosis made?

The patient or relatives notice increasing difficulty in hearing. One’s own voice may sound loud in the affected ear. When fluid is present, head movements can cause a feeling of fluid moving in the ear.

Clinical E.N.T. Examination show the ear drum on the affected side/sides to be moving poorly with some parts of the ear drum/drums drawn in. The nose and throat may show evidence of infection or allergy. Enlarged adenoids or other growth of the nasopharynx may be noted.

For assessing, nose, nasopharynx and paranasal sinus conditions, a C. T. Scan with (usually without injection of contrast dye material) of these areas may be necessary.

What is the treatment?

Treatment is aimed at establishing middle ear ventilation by treating the nasal end of the Eustachian tube.

Any nasal infection or allergy has to be treated. The swelling of the lining of the eustachian tube has to be shrunk up by the use of nose drops. This allows to and fro air passage along the eustachian tube. Attempts are made to force air into the middle ear through the eustachian tube actively by the auto inflation exercise (Valsalva maneuver). explained elsewhere. Nasal steroid sprays on a long-term basis may be required in allergic conditions, swollen (edematous) mucous membrane lining and cases with nasal polyp formation.

In a small percentage of patients if middle ear fluid is present, if the above measures do not give relief, surgical treatment is required – a small incision is made in the ear drum under local anaesthesia and the fluid sucked out. If the fluid is very thick, a small ventilation tube (grommet) is inserted through the incision and left in place. It normally takes 3 to 6 months to extrude spontaneously.

Treatment of the nasopharyngeal condition like removal of enlarged adenoids in children or adequate treatment of nasopharyngeal growth is required. Clearance of nose and paranasal sinus disease by Functional Endoscopic Sinus Surgery (F.E.S.S.) may be required.

Detection of allergies by an allergy test followed by proper treatment may be necessary.

Otosclerosis is a disease of the hearing mechanism in the middle (and internal) ear in which the third bone of the chain of 3 bones in the middle ear gradually gets fixed due to new bone formation and decreasing the vibrations of sound entering the inner ear. (see diagram). The cause of the disease is unknown. It usually manifests after the age of 15 years and is commoner in females. In 80 % of cases, the disease affects both ears to a greater or lesser extent.

The patient or relatives notice increasing difficulty in hearing, mainly in one ear. One’s own voice may sound loud and hence the patient tends to speak softly as compared with patients with a weakness of the hearing nerve (sensori neural hearing loss) who tend to speak loudly. In some patients the first complaint is an intermittent or continuous spontaneous noise in the ear (tinnitus).

For some reason, in females, every pregnancy increases the deafness.

As the disease process advances, the otosclerosis can involve the opposite ear (in80% patients). When the inner ear is also affected by the process (cochlear Otosclerosis) a “mixed” deafness (conductive and sensori-neural) develops.

Whites are the most affected race, with the prevalence in the Black and Asian populations being much lower. Females are twice as likely as males to be affected. Usually noticeable hearing loss begins at middle-age, but can start much sooner. The hearing loss often grows worse during pregnancy.

The disease is inherited as an autosomal dominant fashion.

Special tests for hearing

Pure Tone Audiometry shows the exact levels of hearing and confirm a conductive deafness where hearing by bone conduction is better than hearing by air conduction. Acoustic Impedance Bridge studies confirm a fixation of the 3rd bone (Stapes) and also confirm normal middle ear pressure but diminished ear drum movement.

What is the treatment?

The main treatment is surgical. The ear drum is lifted up and the middle ear is entered. Under an operating microscope, the joint between the 2nd bone (Incus) and third bone (Stapes) is separated. The upper part of the Stapes bone (super structure) is removed. A very small microscopic hole of 0.6 to 0.8 mm diameter is made in footplate of the stapes bone (Stapedotomy). One end of a teflon piston is inserted through this hole, either directly or through a vein graft. The other end of the piston is hooked around the 2nd bone (Incus). The ear drum is then replaced back in the original position.

Sound vibrations now travel from the ear drum via the teflon piston.

Hearing is restored to normal on the operating table in 97 to 98% of cases.

A Hearing aid will also give satisfaction, as in any case of conductive deafness. However, it can never give the satisfaction of normal natural hearing as a successful operation does.

Otosclerosis is a slowly progressive disease. As years go by, deafness increases and the opposite ear too shows signs of involvement. In females, every pregnancy increases the deafness. Gradually, after the age of 45 or 50 years, when old age deafness sets in due to age related changes of the nerves of hearing, the hearing impairment becomes more pronounced and a definite handicap in communication.

Treatment of otosclerosis relies on two primary options: hearing aids (more recently including bone-conduction hearing aids) and a surgery called a stapedectomy. Hearing aids are usually very effective early in the course of the disease, but eventually a stapedectomy may be required fordefinitive treatment. Early attempts at hearing restoration via the simple freeing the stapes from its sclerotic attachments to the oval window were met with temporary improvement in hearing, but the conductive hearing loss would almost always recur. A stapedectomy consists of removing a portion of the sclerotic stapes footplate and replacing it with an implant that is secured to the incus. This procedure restores continuity of ossicular movement and allows transmission of sound waves from the eardrum to the inner ear.

A modern variant of this surgery called a stapedotomy, is performed by drilling a small hole in the stapes footplate with a micro-drill or a laser, and the insertion of a piston-like prothesis. The success rate of either a stapedotomy or a stapedectomy depends greatly on the skill and the familiarity with the procedure of the surgeon.

Other less successful treatment includes fluoride administration, which theoretically becomes incorporated into bone and inhibits otosclerotic progression. This treatment cannot reverse conductive hearing loss, but may slow the progression of both the conductive and sensorineural components of the disease process. Recently, some success has been reported with bisphosphonate medications, which stimulate bone-deposition without stimulating bony destruction.

Blow your nose as you would to clear nasal discharge, however with thumb and index finger pinching and shutting off both nostrils. Close mouth tight. Puff up your cheeks and blow nose to force air gently into your ears.

When performed successfully, you will feel air enter your ear / ears with a click with improvement in hearing.

Today, radiology and imaging includes a large number of modalities and covers virtually all organs in the body. It is virtually impossible for any one individual to keep abreast of all developments and to be as good in all of them.

We, at Jankharia Imaging, have subspeciality training in specific organ systems and modalities and each one of us is an expert in our area of expertiseToday, radiology and imaging includes a large number of modalities and covers virtually all organs in the body. It is virtually impossible for any one individual to keep abreast of all developments and to be as good in all of them.

There are many situations in which, after you have had a radiology examination performed (e.g., x-ray, mammogram, bone densitometry, CT scan or MRI), you may feel the need for another opinion. The reasons may include one or more of those listed below:

When assurance is need about the report’s conclusions from another expert radiologist

When a subspeciality opinion is required as against that of a generalist

When the case is complex, and a diagnosis has not yet been reached

Radiology Opinions

Using our expertise, we will read your examinations, sent to us on CT, films or via the Internet, as the case may be and will get back to you within two working days at the most. We are happy to receive examinations from

A drop attack is a sudden fall, with or without unconsciousness, due either to collapse of muscle tone or abnormal muscle contraction in the legs. Many neurological diseases, cardiac diseases, ear diseases, muscle dysfunction conditions like myoclonic syndromes and startle responses can cause drop attacks. In about 30% of drop attacks the cause is unknown.

Weakness of muscles of the legs

Weakness of the hip and knee extensor muscles (important for maintaining an erect posture)
Some causes include muscular dystrophy, neurogenic atrophy, polymyositis, myasthenia gravis and spinal cord ischemic attacks. Duchenne’s muscular dystrophy is the most common cause of muscle dystrophy.

Isolated quadriceps weakness – secondary to diseases like polymyositis, inclusion body myositis and neurogenic atrophy, and the legs may suddenly give way without warning to cause falls

Intermittent spinal ischemia can produce sudden attacks of transient paraparesis or falls, and causes include syphilitic arteritis, arteriosclerosis of the distal aorta, adhesive arcachnoiditis, spinal compression due to spinal stenosis or disc herniation; the attacks are often precipitated by exercise and relieved by rest

Neurodegenerative diseases

Patients with Parkinson’s disease often fall due to defective postural reflexes, sudden freezing, and uncoordinated turning; their stooped flexed posture predisposes them to falling forward because their centre of gravity is displaced forward when standing or walking.
Other neurodegenerative diseases associated with frequent falls include progressive supranuclear palsy, corticobasal degeneration, Huntington’s chorea, multiple system atrophy and Alzheimer’s disease

Transient ischemic attacks
A patient with vertebro-basilar artery ischemia can present with a sudden loss of tone in their legs, causing their knees to buckle. The patient falls powerlessly without protective arm movements; There may be no precipitating head or neck movements or loss of consciousness, The patient can get up and walk immediately or within one minute. Usually other symptoms of brainstem ischemia are present (vertigo, diplopia, blurred vision, sensory changes, motor weakness, which suggest the diagnosis.

Epilepsy
Drop attacks can be due to sudden muscle contractions associated with generalized convulsive epilepsy, or a sudden loss of postural tone due to atonic epilepsy or epileptic negative myoclonus.
Atonic epileptic attacks in children can occur when standing or sitting or lying, and there is no aura or state of confusion; sudden drop attacks can cause the patient to collapse with triple flexion of the legs and no involvement of the arms. The patient can usually get up immediately after an attack.

Various myoclonic syndromes
Mycoclonus is a sudden brief, shock-like muscle movement caused by a brief muscle contraction (positive myoclonus) or inhibition of a muscle contraction (negative myoclonus)
It can mimic idiopathic drop attacks, and the patient can fall suddenly with buckling of the legs

Startle reactions
Pathological startle reactions (hypereflexia) are characterized by an exaggerated motor response to unexpected auditory stimuli, and less frequently to visual or somasthetic stimuli.
They consist of both brief myoclonic jerks and longer tonic spasms
Hypereflexia may have a variety of causes eg. idiopathic, hereditary, or secondary to acquired brainstem diseases – post-anoxic encephalopathy, viral or paraneoplastic brainstem encephalitis, multiple sclerosis, sarcoidosis or brainstem strokes. Myoclonic jerks occur frequently during the day, but also at night when the patient is asleep, and mainly affect the legs
Sterotyped tonic spasms consist of facial grimacing, flexion of the neck and trunk, flexion or extension of the hips and knees, and characteristic abduction of the shoulders with flexion of the elbows. The patient falls forwards rigidly like a log, but sometimes falls backwards; protective reflexes are impossible and injuries common; consciousness is maintained during the fall and recovery is fast

Cataplexy and paroxysmal choreoathetosis
Cataplexy can cause sudden falls without LOC, but the patient cannot speak during the fall
Characteristic precipitating factors include laughter or a sudden emotional stimulus. Minor symptoms of cataplexy may consist of a brief drop of the jaw and sagging of the head, but severe attacks can cause loss of tone in all the antigravity muscles and the patient falls powerlessly and loosely and remains immobile for many seconds (longer than in hypereflexia)

Paroxysmal choreoathetosis – attacks are usually precipitated by sudden leg movements during standing or running or social embarrassment => the patient may suddenly lose control due to tonic spasms or an involuntary choreoathetotic muscle movement and fall like a log

Meniere’s drop attacks (Tumarkin’s otolithic crisis)
Seen in the early or late stages of Meniere’s disease when there is a sudden change in endolymphatic pressure which causes end-organ stimulation with a reflex-like vestibulospinal loss of postural tone. The patient suddenly loses control of balance and falls and he sometimes with a distinct feeling of being pushed or thrown to the ground. The patient does not lose consciousness.
(* a patient with Wallenberg’s syndrome, due to a lateral medullary stroke, may have a similar transient sensation of being pulled or pushed to the side, and the patient suddenly falls to the side without realizing that it is his active shift of the centre of gravity – lateropulsion – that causes the momentary imbalance)

Idiopathic drop attacks (no specific cause found)
A fall without warning, not associated with loss of consciousness, not apparently due to any malfunction of the legs, not induced by changes of posture or movement of the head, and not accompanied by vertigo or other cephalic sensation, and not associated with myoclonic jerks
It usually appears between the ages 40 – 60 years. Patients only fall when standing or walking, and they usually buckle at the knees and fall forwards.
The attacks occur very suddenly and the patient cannot remember if he lost consciousness, or not; the patient can get up immediately unless accidental injury occurs (minor upper limb fractures and/or dislocations are common in the elderly)
Serial attacks are rare, and spontaneous remission is common (25 – 80%)

Superior canal dehiscence syndrome (SCDS) is a rare condition of the inner ear, first described in 1998 by Dr.Lloyd Minor of Johns Hopkins University, Baltimore, USA, leading to hearing and balance disorders in those affected. The symptoms are caused by a thinning or complete absence of the part of the temporal bone overlying the superior semi circular canal. This may result from slow erosion of the bone or physical trauma to the skull and there is evidence that the defect or susceptibility is congenital.
Symptoms

• Autophony – Patients with SCDS-related autophony report hearing their own voice as a disturbingly loud and distorted sound deep inside the head as if relayed through “a cracked loudspeaker.” Additionally they may hear the creaking and cracking of joints, the sound of their footsteps when walking or running, their heartbeat and the sound of chewing and other digestive noises. A distinctive feature of this condition almost exclusively associated with SCDS is hearing the sound of the eyeballs moving in their sockets (e.g. when reading in a quiet room) “like sandpaper on wood”.
• Tullio phenomenon, another of the more identifiable symptoms leading to a positive SCD diagnosis is sound-induced loss of balance. Patients showing this symptom may experience vertigo, a feeling of motion sickness or even actual nausea, triggered by normal everyday sounds. Although this is often associated with loud noises, volume is not necessarily a factor. Patients describe a wide range of sounds that affect balance: a telephone ringing; a knock at the door; music; the sound of children playing and even the patient’s own voice are typical examples of sounds that can cause a loss of balance when this condition is present, although there are countless others. For such persons, a visit to the concert hall or to a noisy playground may seem like being at the epicenter of an earthquake. A change of pressure within the middle ear (for example when flying or nose-blowing) may equally set off a bout of disequilibrium or nystagmus.
• Low-frequency conductive hearing loss is present in many patients with SCDS and is explained by the dehiscence acting as a “third window.” Vibrations entering the ear canal and middle ear are then abnormally diverted through the superior semi circular canal and up into the intracranial space instead of being registered as sound in the hearing center, the cochlea. This hearing loss being greater in the lower frequencies and may initially be mistaken for otosclerosis.

• Pulsatile tinnitus is yet another of the typical symptoms of SCDS and is caused by the gap in the dehiscent bone allowing the normal pulse-related pressure changes within the cranial cavity to enter the inner ear abnormally. This pressure change thus becomes audible and an existing tinnitus will be perceived as containing a pulse-synchronized “wave” or “blip” which patients describe as a “swooshing” sound.
• Brain fog and fatigue are both common SCDS symptoms and are caused by the brain having to spend an unusual amount of its energy on the simple act of keeping the body in a state of equilibrium when it is constantly receiving confusing signals from the dysfunctional semicircular canal.
• Headache and migraine are also often mentioned by patients showing other symptoms of SCDS. A direct causal link has yet to be proven. Causes
In approximately 2.5% of the general population the bones of the head develop to only 60-70% of their normal thickness in the months following birth. In SCDS the section of temporal bone separating the superior semicircular canal from thecranial cavity, normally 0.8 mm thick, shows a thickness of only 0.5 mm, making it more fragile and susceptible to damage through physical head trauma or from slow erosion.

Diagnosis
The presence of dehiscence can be detected by a high definition (0.6 mm or less) coronal CT Scan of the temporal bone, currently the most reliable way to distinguish between superior canal dehiscence syndrome (SCDS) and other conditions of the inner ear involving similar symptoms such as Meniere’s disease and Perilymph fistula. Other diagnostic tools include the VMPtest, CENG (Computerized ElectroNystagmography) or VNG, electrocochleography (ECOG) and the rotational chair test. An accurate diagnosis is of great significance as unnecessary exploratory middle ear surgery may thus be avoided. Several of the symptoms typical to SCDS (e.g. vertigo and Tullio) may also be present singly or as part of Ménière’s disease, sometimes causing the one illness to be confused with the other. There are reported cases of patients being affected by both Ménière’s disease and SCDS concurrently.

Treatment
Once diagnosed, the gap in the temporal bone can be repaired by surgical resurfacing of the affected bone or plugging of the superior semicircular canal. These techniques are performed by accessing the site of the dehiscence either via a middle fossa craniotomy or via a canal drilled through the transmastoid bone behind the affected ear.